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Ann Robinson Endowed Chair in Psychiatry, Professor and Chairman, Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School; Attending Psychiatrist, Sentara Norfolk General Hospital, Norfolk, Va.

First published in Psychiatry Weekly, Volume 8, Issue 24, December 2, 2013

Introduction

Increasingly, the pathogenesis of attention-deficit/hyperactivity disorder (ADHD) is thought to include inefficient synaptic transmission between widely distributed nodes in the brain, broadening the focus beyond dysregulated frontostriatal circuits.¹

It is clear that childhood symptoms of ADHD can persist into adulthood, often contributing to poor functional outcomes. Consistent with this view of disrupted or inefficient connectivity across broadly separated regions of the brain, a recent diffusion tensor imaging (DTI) study examining fractional anisotropy (FA) in 51 adult white males (mean age 41.3 years; SD 2.8 years) with unambiguous diagnostic assignment of ADHD in childhood (mean age 8.3 years; SD 1.6 years) suggested abnormalities of white matter tracts persisted from childhood into adulthood, irrespective of ADHD remission status in adulthood.¹ The controls were 66 age-matched adult males (age 41.2 years; SD 3.1 years) who had been followed since about 18 years of age.

History of Pediatric ADHD and Fractional Anistropy

FA is a measure that ranges from 0, when water is equally likely to diffuse in all directions because there are no barriers to its movement, to 1, when the diffusion of water is restricted to only one direction. When white matter tracts are intact, the directional diffusion of water is restricted by myelin, membranes, and the density of axons within the white matter tracts, and the value of FA is high. When white matter tracts are disrupted, however, the direction of the diffusion of water is less restricted and the value of FA is lowered. The fundamental assumption underlying DTI tractography is that the principal direction of water diffusion informs the orientation of axons.

In the present study, the adult probands with childhood histories of ADHD showed significantly lower values of FA than the controls without childhood histories for several clusters of tracts in the left and right hemispheres.¹ Specifically, in the left hemisphere, the following tracts had lower FA: the left inferior fronto-occipital fasciculus, which may account for problems with attention set-shifting abilities; the left inferior longitudinal fasciculus, underlying possible subtle disruption of visual perception and object recognition; and the left posterior thalamic radiation, suggesting subtle disruption of communication between the lateral geniculate nucleus and the occipital lobe. As underscored by the authors, these data should stimulate greater examination of dysfunctions of the visual system in ADHD, especially early visual processing.

"Adult probands with childhood histories of ADHD showed significantly lower values of fractional anistropy than controls for several clusters in the left and right hemispheres."

The following tracts in the right hemisphere had lower FA values: the right superior longitudinal fasciculus II, which connects the dorsolateral prefrontal cortex and inferior parietal lobe and may contribute to problems with spatial orientation and spatial working memory; and the right superior and posterior corona radiata, whose subtle disruption may contribute to sensorimotor deficits.

Interestingly, in prior work, the investigators found that several regions with reduced cortical thickness in adults with childhood histories of ADHD were connected by the white matter tracts with lower FA. The data also suggested that, relative to the adult controls without childhood histories, FA was reduced in the right anterior corona radiata in probands with persistent ADHD into adulthood, which contains fibers connecting the anterior cingulate cortex and striatum. Because the dorsal anterior cingulate cortex is involved in functions that are disrupted in ADHD (eg, attention, response selection, error detection, and motivation), there is interest in the possible contributions disruption of the right anterior corona radiata can make to presentations of ADHD.

Conclusions

DTI tractography may reveal how inefficient synaptic transmission between widely-distributed areas of brain due to subtle structural abnormalities of white matter tracts leads to clinical presentations of ADHD and other neurodevelopmental disorders.¹ However, persistent white matter tract abnormalities in remitted adults with childhood histories of ADHD suggest that the brain may be able to work harder and compensate for inefficient information processing along these subtly disrupted tracts, particularly in adulthood.

Disclosure: Dr. Deutsch has received grant support from the Commonwealth Health Research Board (State of Virginia).

References:

1. Cortese S, Imperati D, Zhou J, et al. White matter alterations at 33-year follow-up in adults with childhood attention-deficit/hyperactivity disorder. Biol Psychiatry. 2013;74:591-598.

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